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59 Cards in this Set
- Front
- Back
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What is the function of the epithelial cells in the gastrointestinal (GI) tract?
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Epithelial cells are specialized in different parts of the GI tract for secretion or absorption.
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What are the different types of muscle in the GI tract? What are their functions?
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Muscularis mucosa: contraction causes a change in the surface area for secretion or absorption.
Circular muscle: contraction causes a decrease in diameter of the lumen of the GI tract. Longitudinal muscle: contraction causes shortening of a segment of the GI tract. |
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What consists of the enteric nervous system of the GI tract? Where are they located?
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Submucosal plexus (Meissner's): between submucosa and circular muscle
Myenteric plexus (Auerbach's): between circular and longitudinal muscle |
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What innervates the GI tract?
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Extrinsic innervation: para and sympathetic nervous systems
Intrinsic innervation: enteric nervous system |
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What makes up the parasympathetic nervous system of the GI tract? What structures do they innervate?
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Vagus nerve innervates the esophagus, stomach, pancreas, and upper large intestine.
Pelvic nerve innervates the lower large intestine, rectum, and anus. |
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What does the intrinsic innervation control?
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Myenteric plexus: primarily controls the motility of the GI smooth muscle.
Submucosal plexus: primarily controls secretion and blood flow. |
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What are the four "official" GI hormones?
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Gastrin
Cholecystokinin (CCK) Secretin Glucose-dependent insulinotropic peptide (GIP) |
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What are the actions of gastrin?
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1) Increases H+ secretion by the gastric parietal cells
2) Stimulates growth of gastric mucosa by stimulating the synthesis of RNA and new protein. |
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What changes are seen in patients with gastrin-secreting tumors?
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Patients with gastrin-secreting tumors have hypertrophy and hyperplasia of the gastric mucosa, due to the stimulation of RNA and protein synthesis by gastrin.
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Where is gastrin secreted from? What is the stimuli for the secretion of gastrin?
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Gastrin is secreted from G cells of the gastric antrum.
Gastrin is secreted in response to: a) small peptides and amino acids in the lumen of stomach b) Distention of the stomach c) Vagal stimulation, mediated by gastrin-releasing peptide (GRP) |
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What inhibits gastrin secretion?
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H+ in the lumen of the stomach inhibits gastrin release (negative feedback).
Somatostatin inhibits gastrin release. |
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What is CCK homologous to? Where does the biologic activity of CCK arise from?
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CCK is homologous to gastrin (the five C-terminal amino acids are the same).
The biologic activity of CCK resides in the C-terminal heptapeptide. |
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What are the actions of CCK?
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1) stimulates contraction of the gallbladder and simultaneously causes relaxation of the sphincter of Oddi for secretion of bile.
2) stimulates pancreatic enzyme secretion. 3) Potentiates secretin-induced stimulation of pancreatic HCO3- secretion. 4) Stimulates growth of the exocrine pancreas. 5) Inhibits gastric emptying |
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Where is CCK released from?
What are the stimuli for release of CCK? Why do TGs not stimulate CCK release? |
CCK is released from the I cells of the duodenal and jejunal mucosa by:
1) small peptides and amino acids 2) Fatty acids and monoglycerides. Triglycerides do not stimulate the release of CCK because they cannot cross intestinal cell membranes. |
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What are the actions of secretin?
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Secretin reduces the amount of H+ in the lumen of the small intestine.
1) Stimulates pancreatic HCO3- secretion and increases growth of the exocrine pancreas. Pancreatic HCO3- neutralizes H+ in the intestinal lumen. 2) Stimulates HCO3- and H2O secretion by the liver, and increases bile production. 3) Inhibits H+ secretion by gastric parietal cells. |
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Where is secretin released from?
What are the stimuli for secretin release? |
Secretin is released by the S cells of the duodenum in response to:
1) H+ in the lumen of the duodenum 2) Fatty acids in the lumen of the duodenum |
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What are the actions of glucose-dependent insulinotropic peptide (GIP)?
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1) Stimulates insulin release from the pancreas in the presence of an ORAL glucose load (oral glucose is more effective than IV in causing insulin release).
2) Inhibits H+ secretion by gastric parietal cells. |
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Where is GIP released from? What are the stimuli for GIP release?
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GIP is secreted by the duodenum and jejunum.
GIP is the only GI hormone released in response to fat, protein, and carbohydrate. |
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What are the GI paracrine enzymes? What are their functions?
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Somatostatin: inhibits the release of all GI hormones
Histamine: increases gastric H+ secretion |
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What are the GI neurocrines? What are their functions?
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VIP: produces relaxation of the GI smooth muscle (including the lower esophageal sphincter); stimulates pancreatic HCO3- secretion and inhibits gastric H+ secretion.
GRP (bombesin): stimulates gastrin release from G cells. Enkephalins: stimulate contraction of GI smooth muscle; inhibit intestinal secretion of fluid and electrolytes. |
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What are slow waves?
Where do they originate from? |
Oscillating membrane potentials that occur spontaneously in the GI tract.
They originate from the interstitial cells of Cajal, the pacemaker of the GI smooth muscle. |
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What is the lowest frequency of slow waves/contractions? Highest frequency?
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Stomach: 3 slow waves/min
Duodenum: 12 slow waves/min |
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Where does the swallowing reflex originate?
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The swallowing reflex is coordinated in the medulla. Fibers in the vagus and glossopharyngeal nerves carry information between the GI tract and the medulla.
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What is "receptive relaxation"? What GI hormone participates in this?
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"Receptive relaxation" is a vagovagal reflex that is initiated by distention of the stomach and is abolished by vagotomy.
The orad region of the stomach relaxes to accomodate the ingested meal. CCK participates by increasing the distensibility of the orad (top) stomach. |
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What is the gastrocolic reflex?
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The presence of food in the stomach increases the motility of the colon and increases the frequency of mass movements.
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What are the functions of saliva?
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1) Initial starch digestion by α-amylase (ptyalin) and initial triglyceride digestion by lingual lipase
2) Lubrication of the ingested food by mucus 3) Protection of the mouth and esophagus by dilution and buffering of ingested foods. |
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What is the composition/characteristics of saliva?
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1) High volume
2) High K+ and HCO3- concentrations 3) Low Na+ and Cl- concentrations 4) Hypotonicity 5) Presence of α-amylase, lingual lipase, and kallikrein. |
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What determines the composition of saliva?
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The salivary flow rate. The higher the flow rate, the more saliva resembles plasma.
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What are the three glands that produce saliva?
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Parotid
Submandibular Sublingual |
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How is saliva formed? What effect does aldosterone have?
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The acinus produces an initial saliva with a composition similar to plasma (same concentrations of Na, K, Cl, HCO3).
The ducts modify the initial process by: reabsorbing Na and Cl, and secreting K and HCO3. Aldosterone acts on the ductal cells to increase the reabsorption of Na and secretion of K (like in the renal distal tubule). |
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What regulates saliva production?
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Saliva production is increased by both sympathetic and parasympathetic activity. Parasympathetic stimulation (CN VII and IX) is more important though.
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What is the sympathetic innervation of salivary glands?
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Sympathetic receptors on acinar and ductal cells are β-adrenergic.
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What are the gastric cell types, and what do they secrete?
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Parietal cells, located in the body: secrete HCl and intrinsic factor.
Chief cells, located in the body: secrete pepsinogen. G cells, located in the antrum: secrete gastrin |
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What is the mechanism of gastric H+ secretion?
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In parietal cells, CO2 and H2O are converted to H+ and HCO3- via carbonic anhydrase.
H+ is secreted into lumen of stomach by H-K ATPase. Cl is secreted along with H; thus the secreted product is HCl. HCO3- in the cells is absorbed into bloodstream in exchange for Cl- (Cl-HCO3 exchange) |
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What stimulates gastric H+ secretion?
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a) Vagal stimulation (via ACh at M3 receptors; via GRP at G cells)
b) Gastrin c) Histamine d) Potentiating effects of ACh, histamine, and gastrin |
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Where is histamine released from? What is its effect?
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Histamine is released from enterochromaffin-like (ECL) cells in the gastric mucosa and diffuses to the nearby parietal cells.
Histamine stimulates H+ secretion by activating H2 receptors on parietal cells. |
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What inhibits gastric H+ secretion?
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a) Low pH (<3.0) in stomach
b) Somatostatin c) Prostaglandins |
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What are the protective factors (against acid) in the gastric mucosa?
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Mucus, HCO3-, prostaglandins, mucosal blood flow, and growth factors.
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What is the difference between gastric and duodenal ulcers, besides the location?
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Gastric H+ secretion is increased in duodenal ulcers, as opposed to gastric ulcers in which H+ secretion is decreased (secreted H+ leaks back through the damaged gastric mucosa).
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What is the composition/characterization of pancreatic secretion?
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1) High volume
2) Same Na and K concentrations as plasma 3) Much higher HCO3- concentration than plasma 4) Much lower Cl- concentration than plasma 5) Isotonicity 6) Pancreatic lipase, amylase, and proteases |
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What determines the composition of the aqueous component of pancreatic secretions?
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Flow rate.
At low flow rates, pancreatic secretions is mainly Na and Cl. At high flow rates, it is mainly Na and HCO3-. Regardless of rate, pancreatic secretions are isotonic. |
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What stimulates the pancreatic secretions? Where do these stimulations arise from?
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Secretin: secreted by S cells of duodenum in response to H+.
CCK: secreted by I cells of the duodenum in response to small peptides, amino acids, and fatty acids. ACh (via vagovagal reflexes): released in response to H+, small peptides, amino acids, and fatty acids. |
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What is the composition of bile?
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Bile contains bile salts, phospholipids, cholesterol, and bile pigments (bilirubin).
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What substances cause the contraction of the gallbladder?
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CCK
ACh |
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Where and how is bile recycled?
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The terminal ileum contains a Na-bile cotransporter, which is a secondary active transporter that recirculates bile acids to the liver.
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In what form are carbohydrates absorbed?
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Only monosaccharides are absorbed. Carbohydrates must be digested to glucose, galactose, and fructose for absorption to proceed.
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What enzymes break down carbohydrates?
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α-Amylases: hydrolyze 1,4-glycosidic bonds in starch
Maltase, α-dextrinase, and sucrase: hydrolyze oligosaccharides to glucose Lactase, trehalase, and sucrase: degrade disaccharides to monosaccharides. |
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How is glucose absorbed?
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Glucose is transported from the intestinal lumen into the cells by Na-dependent cotransport (SGLT1).
Glucose is transported from cell to blood by facilitated diffusion (GLUT2). |
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How is galactose absorbed? Fructose?
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Galactose is absorbed in the same way as glucose: through SGLT1 cotransporter (with Na), and GLUT2.
Fructose is transported exclusively by facilitated diffusion. First it is absorbed from the lumen with GLUT5, and sent to the blood with GLUT2. It cannot be absorbed against a concentration gradient. |
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What are the enzymes responsible for protein digestion?
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Endopeptidases
Exopeptidases Pepsin Pancreatic proteases (trypsin, chymotrypsin, elastase, carboxypeptidase A and B) |
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How does pepsin function?
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Pepsin is secreted as pepsinogen by the chief cells of the stomach. Pepsinogen is activated to pepsin by gastric H+. The optimum pH for pepsin is 1-3. When pH >5 (as in duodenum, pepsin is denatured.
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How does trypsin function?
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Trypsinogen is activated to trypsin by a brush border enzyme, enterokinase.
Trypsin converts chymotrypsinogen, proelastase, and procarboxypeptidase A and B (and trypsinogen) to their active forms. |
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How are proteins absorbed?
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Proteins can be absorbed as amino acids, dipeptides, and tripeptides.
Na-dependent amino acid cotransport occurs in the luminal membrane. AAs are then transported from cell to blood by facilitated diffusion. Dipeptides and tripeptides are absorbed through H+-dependent cotransport. In intestinal cells, cytoplasmic peptidases hydrolyze them to amino acids. |
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What do the lipases do?
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Lingual lipases digest some of the ingested triglycerides to monoglycerides and fatty acids.
Pancreatic lipases hydolyze lipids to fatty acids, monoglycerides, cholesterol, and lysolecithin. |
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What are the pancreatic lipases?
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Pancreatic lipase
Cholesterol ester hydrolase Phospholipase A2 |
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How do micelles function?
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Micelles bring the products of lipid digestion into contact with the absorptive surface of the intestinal cells. Fatty acids, monoglycerides, and cholesterol diffuse across the luminal membrane into the cells. Glycerol is hydrophilic and is not contained in the micelles.
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After transport into the cells, where do the products of lipid digestion go?
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In the intestinal cells, they are re-esterified to triglycerides, cholesterol ester, and phospholipids, and with apoproteins form chylomicrons. These are transported out by exocytosis, and transferred to lymph vessels.
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What are some causes of malabsorption of lipids (steatorrhea)?
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a) Pancreatic disease: pancreas cannot synthesize adequate amounts of enzymes (pancreatitis, cystic fibrosis)
b) Hypersecretion of gastrin c) Ileal resection: leads to a depletion of bile acid d) Bacterial overgrowth: may lead to deconjugation of bile acids and early absorption in small intestine. e) Decreased number of intestinal cells (tropical sprue) f) Failure to synthesize apoprotein B: inability to form chylomicrons (abetalipoproteinemia) |
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How is K absorbed or secreted?
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Dietary K is absorbed in the small intestine by passive diffusion via a paracellular route.
K is actively secreted in the colon, stimulated by aldosterone. |
